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TRANSIENT    AURICULAR 
FIBRILLATION 

An  Electrocardiographic  Study 

Thesis  presented  to  the  Faculty  of  the  Graduate  School  of  the  University  of 

Pennsylvania  in  partial  fulfilment  of  the  requirements 

for  the  degree  of  Ph.D.,  1916. 


BY 


EDWARD    B.  KRUMBHAAR,  M.D. 


(From  the  John  Herr  Musser  Department  of  Research  Medicine, 
University._ol_Eennsylvania,  Philadelphia.) 


OFT 

UN  I  VE  K  3T  TY 

_  _ 

^  '  ! 


CHICAGO 

AMERICAN    MEDICAL    ASSOCIATION 

FIVE    HUNDRED    AND    THIRTY-FIVE    NORTH    DEARBORN    STREET 
1916 


TRANSIENT    AURICULAR 
FIBRILLATION 

An  Electrocardiographic  Study 

Thesis  presented  to  the  Faculty  of  the  Graduate  School  of  the  University  of 

Pennsylvania  in  partial  fulfilment  of  the  requirements 

for  the  degree  of  Ph.D.,  1916. 


BY 

EDWARD    B.  KRUMBHAAR,  M.D. 


(From  the  John  Herr  Musser  Department  of  Research  Medicine, 
University  of  Pennsylvania,  Philadelphia.) 


CHICAGO 

AMERICAN    MEDICAL    ASSOCIATION 

FIVE    HUNDRED    AND    THIRTY-FIVE    NORTH    DEARBORN    STREET 
1916 


B)C 
UBHARY 


TRANSIENT    AURICULAR    FIBRILLATION 

AN    ELECTROCARDIOGRAPHIC    STUDY  * 
EDWARD    B.    KRUMBHAAR,    M.D. 

PHILADELPHIA 

In  this  communication  are  presented  the  results  of  a  detailed  study, 
by  means  of  the  electrocardiograph,  of  six  individuals  exhibiting  the 
change  from  a  normal  heart  rhythm  to  that  of  auricular  fibrillation. 
Although  the  disturbance  of  cardiac  mechanism  that  causes  this  type 
of  cardiac  irregularity — incoordinate  contraction  or  fibrillation  of  the 
auricular  musculature — has  been  understood  only  during  the  past  few 
years,  its  clinical  prototype,  the  pulsus  irregularis  perpetuus  of  Hering, 
or  the  totally  irregular  pulse,  has  for  years  been  recognized  as  one  of 
the  commonest  as  well  as  one  of  the  gravest  forms  of  cardiac  arrhyth- 
mia. Perhaps  from  the  widespread  use  of  Hering's  terminology,  how- 
ever, the  erroneous  impression  has  been  prevalent  that  this  condition 
once  present  is  practically  always  permanent.  Already  a  sufficient  num- 
ber of  cases  have  been  published  to  combat  this  view,  so  that  we  must 
now  consider  that  auricular  fibrillation,  like  the  other  disturbances  of 
the  cardiac  mechanism — premature  contractions,  heart  block  and  alter- 
nation— may,  though  less  frequently,  occur  in  a  transitory  as  well  as  a 
permanent  form.  My  main  thesis  will  be  to  show  not  only  that  tran- 
sient auricular  fibrillation  constitutes  a  well  recognized  condition,  but 
that  it  may  be  subdivided  into  three  well-defined  groups. 

REVIEW  OF  THE  LITERATURE 

Cushny  and  Edmunds,1  in  the  paper  that  first  propounded  the  theory 
that  a  totally  irregular  pulse  is  due  to  fibrillation  of  the  auricles,  were 
led  to  their  experimental  work  by  the  study  of  a  woman  who  had  had 
numerous  paroxysmal  attacks  of  fibrillation  during  several  years  of 
observation.  No  determining  factor  was  discovered  clinically,  but  the 
conclusion  was  reached  that  the  attacks  were  due  to  reflex  vagus  inhi- 
bition. 


*  From  the  John  Herr  Musser  Department  of  Research  Medicine,  Univer- 
sity of  Pennsylvania,  Philadelphia. 

1.  Cushny,  A.  R.,  and  Edmunds,  C.  W. :  Paroxysmal  Irregularity  of  the 
Heart  and  Auricular  Fibrillation,  Am.  Jour.  Med.  Sc.,  1907,  cxxxiii,  66. 


*i  I  >       v 

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Very  similar  cases  have  been  reported  by  Fox,2  Hornung,3  G.  C. 
Robinson,4  Popper,5  and  Lewis  and  Schleiter.6  These  patients,  as  was 
Cushny  and  Edmund's  patient,  were  all  over  50  years  of  age  and  had 
had  numerous  attacks,  lasting  from  a  few  minutes  or  hours  to  several 
days,  and  extending  over  many  years.  In  none  was  a  valvular  defect 
present,  but  hypertension  and  preponderance  of  the  left  ventricles  were 
found  in  all.  Another  interesting  group  of  ten  cases  has  been  reported 
by  Heitz,7  together  with  polygraphic  records,  which  unfortunately  do 
not  absolutely  preclude  the  existence  of  some  other  form  of  arrhythmia. 
In  another  series,  out  of  a  total  of  120  patients  with  auricular  fibrilla- 
tion examined  electrocardiographically,  Fahrenkamp8  found  only  four 
in  whom  the  trouble  was  transient  (3.3  per  cent.).  Though  paroxysmal 
in  character,  the  attacks  were  all  single  and  short  (one  fatal),  seen  in 
acute  conditions,  such  as  Graves'  disease,  pneumonia  and  septicemia. 
Further  details  of  these  cases  will  be  considered  later,  in  connection 
with  the  discussion  of  the  cases  here  reported.  The  cases  reported  by 
Falconer  and  Dean9  and  by  Schwarzmann10  developed  transient  attacks 
of  fibrillation  in  the  presence  of  an  already  existing  heart  block.  The 
complication  that  this  causes  makes  it  inadvisable  to  include  them  in 
this  discussion. 

The  older  theory  that  a  temporarily  but  totally  irregular  pulse 
(delirium  cordis)  is  not  uncommon  and  frequently  disappears  under 
digitalis  medication  was  in  most  cases  due  to  imperfect  observation. 
The  probability  is  that  in  such  cases  the  slight  degree  of  arrhythmia, 
which  became  still  less  with  the  improvement  of  the  patient,  became 
unnoticeable  to  the  touch,  in  spite  of  the  fact  that  the  underlying  con- 
dition of  fibrillation  persisted.  In  some  cases,  also,  as  Fahrenkamp  and 
others  have  pointed  out,  the  occurrence  of  complicated  groups  of  extra- 
systoles  may  (in  the  absence  of  electrocardiograms)  present  a  picture 
indistinguishable  from  auricular  fibrillation. 


2.  Fox,  G.  H. :  Transitory  Delirium  Cordis,  Am.  Jour.  Med.  Sc.,  1910,  cxl,  815. 

3.  Hornung,  O. :   Ueber  atypische  tachykardische  Paroxysmen,  Deutsch.  Arch, 
f.  klin.  Med.,  1907,  xci,  469. 

4.  Robinson,  G.  C. :    Paroxysmal  Auricular  Fibrillation,    THE  ARCHIVES  INT. 
MED.,  1914,  xiii,  298. 

5.  Popper,  H. :   Ueber  Anfalle  von  Vorhofflimmern,  Med.  Klin.,  1915,  xi,  885. 

6.  Lewis,  T.,  and  Schleiter,  H.  G. :    The  Relation  of  Regular  Tachycardias 
of  Auricular  Origin  to  Auricular  Fibrillation,  Heart,  1911-1912,  iii,  173. 

7.  Heitz,  J. :    La  forme  paroxystique  de  1'arythmie  complete,  Ann.  de  med., 
1914,  i.  483. 

8.  Fahrenkamp,    K. :     Voriibergehende    komplette    Herzunregelmassigkeiten 
unter   dem   klinischen   Bilde   der  Arythmia   Perpetua   mit   Beobachtungen  iiber 
Vaguswirkung,  Deutsch.  Arch.  f.  klin.  Med.,  1914,  cxvii,  1. 

9.  Falconer,  A.  W.,  and  Dean,  G. :    Observations  on  a  Case  of  Heart  Block 
Associated    with    Intermittent   Attacks   of   Auricular    Fibrillation,    Heart,    1911- 
1912,  iii,  247. 

10.  Schwarzmann.  G.  S. :    Ueber  ein  Fall  von  Herz  Block  mit  Paroxysmalem 
Vorhofflimmern.  Zentralbl.  f.  inn.  Med.,  1914,  xxxv,  1001. 


The  six  cases  of  fibrillation  mentioned  above  are  here  reported  in 
detail,  in  the  hope  that  they  may  throw  some  light  on  the  poorly  under- 
stood pathogenesis  of  this  common  and  serious  condition  and  on  the 
prognosis  of  such  transient  cases.  The  fibrillation  in  four  of  the  cases 
was  found  to  be  transient,  and  in  the  other  two  cases  developed  while 
the  patients  were  under  observation.  These  four  represent  7.5  per  cent, 
of  the  total  number  of  cases  of  auricular  fibrillation  studied  electro- 
cardiographically  at  the  University  Hospital  during  a  period  of  two 


Fig.  1  (Case  1). — Electrocardiogram  of  V.  W.,  showing  transient  auricular 
fibrillation  in  lobar  pneumonia.  In  this,  as  in  other  electrocardiograms  of 
this  series,  records  were  taken  from  the  three  customary  leads.  The  tension 
of  the  string  was  so  standardized  that  1  millivolt  caused  a  deflection  of  1  cm. 
As  the  string  could  not  be  standardized  with  the  patient  in  circuit,  1,400  ohms 
were  added  as  an  arbitrary  equivalent  of  the  patient's  resistance.  Platinum 
string,  resistance  about  3,500  ohms.  Time  intervals  are  expressed  in  fifths  of 
second  and  occasionally  by  vertical  lines  indicating  %  and  ^5  second.  In  this 
figure,  note  (1)  absence  of  sign  of  auricular  contraction  (P  wave)  ;  (2) 
ventricular  arrhythmia  (irregular  occurrence  of  R)  ;  and  (3)  occasional  coarse 
waves  of  fibrillation. 


and  a  half  years.  While  this  is  apparently  an  unusually  high  percen- 
tage of  transient  fibrillation,  it  is  very  probable  that  the  wider  use  of 
graphic  methods  of  registration  will  in  the  near  future  demonstrate  its 
greater  frequency. 


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Fig.  2  (Case  1). — Electrocardiogram  of  same  patient  as  in  Figure  1,  show- 
ing normal  rhythm  during  convalescence  from  pneumonia.  Note  reappear- 
ance of  P  wave,  regular  occurrence  of  R  and  absence  of  fibrillation  waves. 
(The  print  of  Lead  II,  as  in  a  few  other  instances,  has  been  retouched  for 
purposes  of  reproduction.) 

I.  TRANSIENT  AURICULAR  FIBRILLATION  IN  LOBAR  PNEUMONIA 

CASE  1. — V.  M.,  a  white  man,  married,  S3  years  old,  a  tinsmith  by  trade, 
was  admitted  to  the  hospital  March  17,  1915,  on  the  third  day  of  a  typical 
attack  of  lobar  pneumonia,  involving  the  left  lower  lobe.  A  total  arrhythmia 
was  noticed  on  admission,  although  the  patient  had  never  noticed  such  arrhythmia 
before  and  had  never  to  his  knowledge  had  any  previous  cardiac  trouble 
Cardiac  dulness  was  not  increased  and  there  were  no  valvular  murmurs.  Except 


for  two  attacks  of  gonorrhea  twenty-five  years  before,  he  had  never  been 
seriously  ill.  He  had  never  had  rheumatism,  tonsillitis  or  other  fever,  although 
a  later  blood  examination  gave  a  positive  Wassermann  reaction.  The  systolic 
blood  pressure  on  admission  was  120,  diastolic  95.  After  the  reestablishment 
of  normal  rhythm,  the  systolic  pressure  was  115,  diastolic  85. 

An  electrocardiogram  (Fig.  1)  taken  on  the  day  of  admission  showed  the 
presence  of  auricular  fibrillation  (of  the  coarse  type),  absence  of  the  P  wave, 
and  a  moderate  degree  of  arrhythmia.  The  form  of  the  electrocardiogram 
shows  no  other  deviation  from  the  normal,  except  that  the  T  wave  is  inverted 
in  Lead  III.  Tincture  of  digitalis  (0.6  c.c.  three  times  a  day)  was  begun  at 
once  and  continued  during  the  patient's  stay  in  the  hospital  of  more  than  a 
month.  Although  the  pneumonic  crisis  was  reached  in  four  days  after  admis- 
sion, with  normal  resolution  of  the  involved  lobe,  the  pulse  rate  remained  over 
100  for  another  ten  days.  The  arrhythmia  became  less  and  less  marked,  until, 
one  month  after  admission,  with  the  pulse  rate  varying  between  60  and  90, 
arrhythmia  was  imperceptible.  An  electrocardiogram  (Fig.  2)  taken  at  this 
time  showed  a  regular  rhythm,  with  the  reappearance  of  the  P  wave.  The 
T  wave  in  Lead  III  is  no  longer  inverted  and  is  more  pronounced  in  the  other 
two  leads  than  in  the  former  record.  The  patient  was  discharged  in  good 
condition  and  since  then  has  had  no  return  of  any  cardiac  irregularity.  A 
polygram  (Fig.  3)  taken  three  months  later  revealed  a  regular  radial  pulse 
(rate  62  beats  per  minute)  with  a  normal  jugular  pulse.  The  fact  that  the 
myocardium  had  not  yet  returned  to  normal,  however,  was  shown  by  the 
persistence  of  pretibial  edema  and  dyspnea  on  exertion. 


4  Fig.  3  (Case  1). — Normal  polygram  three  months  after  pneumonia.  Note 
regular  radial  rhythm  and  normal  "a,  c,  v"  type  of  venous  pulse,  with  promi- 
nent "a"  wave. 

Summary  of  Case. — A  patient  in  the  third  day  of  an  attack  of  lobar 
pneumonia  was  found  to  have  auricular  fibrillation  with  considerable 
arrhythmia,  although  there  had  been  no  previous  history  of  heart  dis- 
ease. After  recovery  from  the  pneumonia,  the  arrhythmia  gradually 
decreased,  until  one  month  later  the  electrocardiogram  showed  a  nor- 
mal P  wave  and  regular  rhythm.  The  exact  time  at  which  the  auricle 
began  again  to  beat  coordinately  was  not  determined,  but  was  appar- 
ently not  accompanied  by  any  noticeable  subjective  symptoms  or  change 
in  rate.  That  the  return  to  a  normal  rhythm  was  permanent  is  shown, 
by  polygraphic  records  taken  three  months  later. 

II.    TRANSIENT    AURICULAR    FIBRILLATION    OF    NERVOUS    ORIGIN    IN 
SYPHILITIC  MYOCARDITIS 

CASE  2. — B.  A.,  a  white  woman,  married,  38  years  old,  was  admitted  to  the. 
hospital  March  2,  1915,  for  the  removal  of  a  uterine  fibroid.  She  had  had 
measles,  mumps,  appendicitis  and  typhoid,  but  had  totally  recovered  from  each, 
and  had  otherwise  been  healthy.  Her  husband  was  living  and  well,  but  she. 
had  had  no  children,  one  miscarriage,  and  the  Wassermann  reaction  was. 
strongly  positive.  She  had  never  complained  of  any  cardiac  trouble  until  three^ 


weeks  before  admission,  at  which  time  after  a  hard  day's  work  she  had  an 
attack  of  palpitation,  dyspnea  and  irregular  heart  action.  Another  attack 
occurred  the  next  evening  and  the  symptoms  continued  more  or  less  marked 
until  admission  to  the  hospital.  On  the  day  of  admission  she  had  a  similar 


Fig.  4  (Case  2). — Electrocardiogram  of  Mrs.  B.  A.,  taken  March  2,  1915, 
showing  transient  auricular  fibrillation  in  syphilitic  myocarditis.  Note  same 
disturbances  of  mechanism  as  in  Figure  1. 

attack,  but  more  serious  than  any  previous  one,  and  the  extreme  rapidity  and 
irregularity  of  the  heart  action  necessitated  the  abandonment  of  the  operation. 
The  patient  attributed  this  attack  to  the  nervous  excitement  aroused  by  con- 
templation of  the  operation. 


At  the  time  of  the  electrocardiographic  study  she  was  in  a  very  nervous 
state,  with  warm,  flushed  skin,  and  marked  tremor  of  the  hands.  The  radial 
pulse  was  distinctly  irregular,  rapid  (180  per  minute),  quick,  full,  with  increased 
tension,  the  wall  slightly  sclerotic.  The  cardiac  dulness  was  slightly  increased 


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Fig.  5   (Case  2). — Electrocardiogram  of  same  patient  as  in  Figure  4,  taken 
March  3,  showing  normal  rhythm. 

to  the  left,  the  apex  beat  distinct  in  fifth  space,  12  cm.  from  the  mid- 
line.  There  was  a  distinct  apical  systolic  murmur  transmitted  to  the  axilla, 
with  accentuated  second  aortic  and  pulmonic  sounds.  An  electrocardiogram 
(Fig.  4)  showed  the  arrhythmia  to  be  due  to  an  auricular  fibrillation  of  the 


10 

coarse  type.  With  the  fear  of  operation  removed,  and  after  a  quiet  night  in 
bed,  the  patient  awoke  the  next  morning  without  any  disagreeable  subjective 
sensations,  and  the  pulse  was  regular  and  much  slower.  The  systolic  blood  pres- 
sure, which  during  the  attack  of  fibrillation  had  been  165,  was  found  during  the 
period  of  regular  rhythm  to  be  132.  The  diastolic  fell  from  85  to  78. 


No. 


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Fig.  6  (Case  2). — Electrocardiogram  of  same  patient  as  in  Figure  4,  taken 
March  9,  showing  normal  rhythm  occasionally  disturbed  by  an  auricular  pre- 
mature contraction. 

An  electrocardiogram  (Fig.  5)  taken  the  same  morning  showed  a  regular 
rhythm,  with  a  normal  P  wave.  The  complexes  were  practically  the  same  as 
in  the  former  record  (the  more  rapid  passage  of  the  film  being  shown  by  the 
increased  intervals  of  the  time  marker),  except  that  systole  (as  indicated  by 


11 

the  end  of  T)  lasted  more  than  0.3  second  and  was  immediately  followed  by 
thg  next  P  wave.  For  several  days  the  patient's  improvement  continued,  the 
pulse  being  either  quite  regular  or  showing  only  an  occasional  slight  irregu- 
larity. The  nature  of  this  irregularity  is  shown  in  Figure  6  to  be  due  to  an 
occasional  extrasystole.  Although  there  is  practically  a  complete  compensatory 
pause,  this  is  probably  an  auricular  extrasystole  merging  with  the  preceding 
T,  because  the  following  ventricular  complex  shows  no  ectopic  origin. 


Fig.  7  (Case  2). — Electrocardiogram  of  same  patient  as  in  Figure  4,  taken 
March  10,  showing  another  period  of  transient  auricular  fibrillation. 

After  one  week's  improvement,  the  patient  awoke  one  morning  from  a  ter- 
rifying dream,  and  felt  her  heart  pounding  violently.  Auscultation  disclosed  a 
total  arrhythmia,  with  disappearance  of  all  murmurs,  a  cardiac  rate  of  130, 
and  a  pulse  deficit  of  50.  The  systolic  pressure  was  found  to  have  risen  to 
155,  the  diastolic  remaining  at  70.  An  electrocardiogram  (Fig.  7)  showed  that 


12 

coarse  fibrillation  had  again  supervened.  In  Lead  I,  especially,  the  fibrillatory 
waves  were  so  marked  and  regular  that  at  first  the  condition  of  auricular  flutter 
was  suggested.  This  was  rejected,  however,  as  the  rhythm  of  the  waves  of 
fibrillation  was  not  absolutely  regular  and  the  ventricular  response  was  totally 
irregular,  and  not  explainable  by  any  combination  of  heart  block.  During  the 
same  afternoon,  the  patient  suddenly  announced  that  the  trouble  had  stopped, 
and  the  rate  was  found  to  be  much  slower  (80  per  minute)  and  less  irregular. 
Occasional  extrasystoles,  however,  persisted  for  forty-eight  hours.  After  one 
week  of  normal  heart  action,  the  patient  was  returned  to  the  surgical  wards 
for  myomectomy  and  from  this  time  on  she  flatly  refused  to  allow  further 
cardiac  examination. 

It  is  of  interest  that  the  patient  later  volunteered  the  information  that  she 
had  had  a  strong  psychic  disturbance  before  each  cardiac  attack.  It  is  of 
course  possible  for  a  third  and  unknown  factor  to  have  been  responsible  for 
both  the  nightmare  and  the  paroxysmal  attack  of  fibrillation,  but  the  pre- 
sumption is  strong  that  the  cardiac  attack  was  induced  by  nervous  excite- 
ment. The  chronic  endocarditis,  enlarged  heart  and  positive  Wassermann  would 
all  indicate  a  basic  myocardial  involvement  requiring  only  the  nervous  excita- 
tion to  produce  the  paroxysm  of  fibrillation.  The  appearance  of  auricular 
extrasystoles  for  a  few  days  after  each  attack  is  also  of  interest.  It  is  impos- 
sible to  say  whether  these  also  were  of  nervous  origin  or  a  sign  of  myocardial 
degeneration,  but  here  again  the  time  of  their  appearance  affords  a  strong 
presumption  that  the  psychic  element  was  at  least  one  factor  in  their  production. 
A  recent  report,  one  year  after  the  period  of  observation,  states  that  the 
patient  is  now  in  a  state  of  chronic  decompensation  and  that  the  arrhythmia 
has  become  permanent. 

Summary  of  Case. — In  a  highly  excitable,  nervous  woman,  on  sev- 
eral occasions  strong  emotional  excitement  was  observed  to  be  followed 
by  transient  attacks  of  auricular  fibrillation.  Though  the  blood  pres- 
sure was  higher  during  the  periods  of  fibrillation,  the  state  of  the  pres- 
sure just  preceding  the  attacks  could  not  be  determined.  After  the  nor- 
mal auricular  activity  had  returned,  the  regular  rhythm  was  disturbed 
for  one  or  two  days  by  occasional  auricular  extrasystoles.  After 
repeated  attacks  during  the  next  year,  the  fibrillation,  which  had  a 
probable  syphilitic  myocarditis  as  a  basis,  became  permanent. 

III.    TRANSIENT   AURICULAR    FIBRILLATION    OF    TOXIC   ORIGIN 

CASE  3. — W.  W.,  a  white  man,  single,  aged  40  years,  was  referred  to  me 
for  examination  on  Oct.  12,  1915,  by  Dr.  Newlin,  on  account  of  extreme 
palpitation,  dyspnea  and  arrhythmia  of  two  days'  duration.  One  brother  had 
died  of  heart  disease,  following  over-indulgence  in  alcohol,  and  there  was  a 
general  family  tendency  toward  overeating  and  overdrinking.  Except  for  occa- 
sional attacks  of  tonsillitis,  the  patient  had  not  had  any  severe  infections,  but  had 
always  eaten  too  much,  and  had  been  a  steady  consumer  of  alcohol,  but  seldom 
to  the  point  of  intoxication.  For  years  he  had  had  some  distress  after  eating 
and  had  occasional  attacks  of  heartburn.  He  had  always  considered  himself 
in  excellent  health,  however,  had  not  overworked,  and  had  been  able  to  under- 
take violent  exercise  without  the  slightest  embarrassment. 

The  present  illness  began  two  months  previously  while  the  patient  was  on 
a  hunting  trip  in  the  Rocky  Mountains  (altitude  5,000  feet).  Following  an 
attack  of  acute  bronchitis,  the  patient  noticed  that  he  easily  became  dyspneic 
and  tired,  and  that  his  heart  occasionally  "skipped"  beats.  The  trip  was  aban- 
doned, and  with  appropriate  treatment  the  symptoms  disappeared.  Systolic 
blood  pressure  at  this  time  was  150.  In  three  weeks'  time  the  patient  felt 


13 

entirely  well,  except  for  a  mild  afebrile  tonsillitis,  which  persisted  for  several 
weeks.  On  a  carbohydrate-poor  diet  he  succeeded  in  losing  50  pounds  and  the 
systolic  blood  pressure  dropped  to  140.  He  then  began  three  days  of  increased 
alcohol  consumption,  and  became  nervous  and  irritable  for  several  days,  but 
without  cardiac  symptoms.  Then  without  adequate  explanation,  after  one  week 
of  total  abstinence,  extreme  palpitation  and  arrhythmia  developed,  with  dizzi- 
ness on  standing.  The  systolic  pressure  at  this  time  was  only  110,  diastolic  90. 
This  attack  had  continued  for  the  two  days  immediately  preceding  his  visit  to 
the  hospital,  but  he  had  improved  sufficiently  to  walk  without  distress. 


Fig.  8  (Case  3). — Electrocardiogram  of  patient  W.  W.,  who  had  no  discover- 
able organic  lesion,  showing  transient  auricular  fibrillation  of  toxic  origin 

Physical  Examination. — The  patient  was  a  large,  powerful,  well-nourished 
man,  weighing  25S  pounds.  Although  normally  rather  lethargic,  he  was  at 
that  time  apprehensive  and  slightly  dyspneic.  The  eyes  were  negative.  The 
tongue  was  moderately  coated,  the  tonsils  red  and  swollen,  but  without  exudate. 
There  were  irregular  heavings  of  the  neck,  but  no  distinct  venous  pulsation. 
The  pulse  rate  was  about  120  and  very  irregular  in  force  and  rhythm.  The 
vessel  wall  was  indefinitely  palpable.  The  heart  rate  by  auscultation  was  160, 
also  irregular  in  force  and  rhythm,  giving  a  pulse  deficit  of  25  per  cent.  The 


14 

'apex  beat  was  not  visible  or  palpable ;  the  cardiac  dulness  extended  to  the 
right  border  of  the  sternum  in  the  fourth  space,  and  1  cm.  to  the  left  of  the 
midclavicular  line  at  the  fifth  space.  No  murmurs  were  audible,  but  the 
muscle  sounds  were  rumbling  and  of  poor  quality.  Examination  of  the  lungs 
and  abdomen  was  negative.  The  legs  showed  very  slight  pitting  on  sustained 
<pressure.  Frequent  urine  examinations  were  always  negative. 


ywA 

I         v    »    *   f 


'     7 


tr*    17      *    fl  V«»uW 


Fig.  9  (Case  3). — The  polygram  taken  immediately  after  the  electrocardio- 
gram shown  in  Figure  8  exhibits  in  a  more  marked  degree  the  irregularities  of 
force  and  rhythm.  The  unmarked  "c"  waves  of  the  jugular  pulse  indicate  the 
'amount  of  pulse  deficit. 


Fig.  10  (Case  3).  —  Electrocardiogram  of  same  patient  as  in  Figure  8,  taken 
three  weeks  later,  showing  normal  rhythm. 


After  three  days'  treatment,  consisting  of  digipuratum  (0.1  gm.  four  times 
a  day)  and  local  applications  to  the  tonsils,  the  patient's  condition  was  greatly 
improved,  with  cessation  of  palpitation,  dyspnea  and  cardiac  distress.  This 


15 

was  confirmed  by  Dr.  Newlin,  who  found  the  heart  action  and  sounds  normal 
and  no  pulse  deficit.  The  systolic  blood  pressure  was  120  and  the  diastolic  80.  As 
a  result  of  this  improvement  the  patient  resumed  his  former  habits  of  over- 
eating and  overdrinking  and  in  seven  months  had  another  cardiac  attack  lasting 
three  days,  which  again  responded  to  digitalis.  This  attack  occurred  in  the 
middle  of  the  night,  while  the  patient  was  trying  to  induce  vomiting  for  the 
relief  of  an  attack  of  heartburn.  At  the  present  time  (May,  1916)  he  has 
headaches,  gets  tired  easily,  and  does  not  feel  so  well  as  before  the  first  attack. 
An  electrocardiogram  (Fig.  8)  taken  on  the  patient's  first  visit  showed  a 
distinct  arrhythmia  with  absence  of  the  P  wave  and  with  the  coarse  type  of 
auricular  fibrillation.  The  delirium  cordis,  however,  was  much  more  strikingly 
shown  in  the  polygraph  (Fig  9)  taken  at  the  same  time,  although  by  this  time  the 
patient  felt  much  better  and  could  not  say  whether  or  not  his  heart  action 
was  irregular.  An  electrocardiogram  (Fig.  10)  taken  three  weeks  later  showed 
a  normal  regular  rhythm  with  well-developed  P  wave.  The  form  of  the 
ventricular  complex  is  but  little  changed  from  that  of  the  former  record. 

Summary  of  Case. — In  an  adult  man,  without  previous  signs  of 
cardiac  disease,  but  with  a  history  of  heartburn  and  chronic  overindul- 
gence in  food  and  alcohol,  signs  of  slight  cardiac  decompensation  devel- 
oped three  months  before  observation.  After  a  short  period  of 
improved  health,  auricular  fibrillation  with  marked  cardiac  symptoms 
developed  without  apparent  adequate  cause.  This  persisted  for  three 
days,  but  disappeared  under  appropriate  treatment  of  rest,  digitalis,  and 
local  treatment  of  a  subacute  tonsillitis,  and  up  to  the  present  time 
(eight  months)  has  not  reappeared,  except  for  one  other  transient 
attack  lasting  for  three  days.  An  underlying  myocardial  weakness  is 
probably  in  this,  as  in  the  other  cases  discussed  in  this  series,  an  impor- 
tant factor.  While  it  is  impossible  absolutely  to  identify  the  determin- 
ing cause  of  the  attack  of  fibrillation,  the  blame  most  probably  must 
fall  on  either  alcohol  or  the  subacute  tonsillitis.  There  were  very  few 
signs  of  decompensation  at  any  time  and  with  the  removal  of  the 
sources  of  intoxication,  the  fibrillation  ceased;  and  yet  on  account  of 
the  probable  myocardial  disease,  a  recurrence  with  correspondingly 
grave  prognosis,  must  be  considered  as  probable. 

IV.  TRANSIENT  AURICULAR  FIBRILLATION  DURING  DECOMPENSATION 

IN   PANCARDITIS 

CASE  4. — J.  P.,  a  white  man,  single,  18  years  old,  was  admitted  to  the  hos- 
pital Feb.  16,  1916,  during  an  attack  of  severe  decompensation,  superimposed 
on  chronic  valvular  disease,  cardiac  hypertrophy  and  chronic  nephritis.  The 
chief  complaints  were  dyspnea,  cough,  edema  of  buttocks  and  extremities. 
Although  cardiac  symptoms  had  been  present  only  four  years  and  then  occurred 
without  determined  adequate  cause,  it  is  probable  that  the  cardiac  disease 
started  during  a  severe  undiagnosed  illness  in  infancy,  which  lasted  eighteen 
months.  He  also  was  said  to  have  had  measles  three  times  during  childhood, 
but  his  past  history  and  family  history  is  otherwise  negative.  Although  he 
had  had  two  or  more  attacks  of  decompensation  before  this,  he  was  "passed" 
by  a  railroad  physician  two  and  one-half  years  before.  The  patient  presented 
the  usual  signs  of  a  decompensated  heart  disease  of  long  standing,  with  flushed 
face,  bulging  precordium,  distended  veins,  tender  liver,  ascites  and  right-side 
hydrothorax.  His  heart  was  enlarged  both  to  the  right  and  to  the  left  and 


16 

a  loud  double  mitral  murmur  was  audible  with  an  accentuated  second  pul- 
monic  sound.  The  systolic  blood  pressure  varied  between  110  and  132;  the 
diastolic  between  93  and  110.  The  venous  blood  pressure  equaled  14  cm. 
(water).  The  urine  has  always  contained  a  large  amount  of  albumin  and 


i" :  f. 


Fig.  11  (Case  4). — Electrocardiogram  of  patient  J.  P.,  a  case  of  fatal  mitral 
stenosis  with  decompensation,  taken  Feb.  29,  1916,  showing  normal  rhythm, 
with  right  ventricular  preponderance. 


occasional  hyaline  casts.  The  phenolsulphonephthalein  elimination  was  40  per 
cent.  The  blood  counts  were  normal.  The  Wassermann  reaction  was  nega- 
tive. An  orthodiagram  showed  increase  of  cardiac  shadow  both  to  the  right 
and  left. 


17 


An  electrocardiogram  (Fig.  11)  taken  the  day  after  admission  showed  a 
regular  rhythm  with  well-defined  P  wave,  and  the  evidences  of  preponderat- 
ing hypertrophy  of  the  right  ventricle  ;  the  P-R  interval  was  0.18  second. 
In  spite  of  absolute  rest  in  bed,  digitalis  and  codein  medication,  the  patient's 


s      s  _J_  = 

No.  4a£zi3x£lz=QQ3zi: 


3£ 


Fig.  12  (Case  4). — Electrocardiogram  taken  March  4,  1916,  of  same  patient 
as  in  Figure  11,  showing  transient  auricular  fibrillation.  Though  the  fibrillation 
has  not  been  of  long  duration,  the  waves  of  fibrillation  are  not  visible. 

condition  became  steadily  worse,  with  increased  edema,  insomnia,  nausea  and 
vomiting.  An  electrocardiogram  (Fig.  12)  taken  twelve  days  later  failed  to  show 
any  change,  and  did  not  show  any  of  Cohn's  digitalis  effects.  A  third  record 
(Fig.  13),  taken  four  days  later,  revealed  the  presence  of  auricular  fibrillation, 


18 

although  no  arrhythmia  was  suspected  until  the  prints  of  this  record  became 
available  for  study.  Another  record  was  taken  three  days  later  and  it  was 
found  that  the  rhythm  had  again  become  regular  with  reappearance  of  the 
P  wave.  The  day  before  this  record  was  made  (that  is,  two  days  after  record- 
ing auricular  fibrillation)  the  signs  of  acute  pericarditis  (loud  to  and  fro  fric- 


"P- K 


I/A  I  O.iSste.. 


Fig.  13  (Case  4). — Electrocardiogram  taken  March  8,  1916,  of  same  patient 
as  in  Figure  11,  showing  normal  rhythm  again,  with  large  P  Wave. 

tion  rub)  became  manifest,  with  increase  in  pulse  rate  (110  to  140),  develop- 
ment of  fever,  and  general  aggravation  of  symptoms.  Although  these  signs 
were  definitely  not  present  in  an  examination  made  the  day  fibrillation  was 
determined,  nevertheless  an  infection,  not  sufficiently  advanced  to  cause  signs, 


19 

cannot  be  ruled  out  as  the  added  insult  that  provoked  the  auricular  fibrillation. 
From  this  time  on  the  patient  became  steadily  worse,  dying  in  four  days  from 
heart  failure. 

At  necropsy  the  following  conditions  were  found :  Concentric  hypertrophy 
of  the  right  ventricle  (weight  270  gm.)  ;  concentric  atrophy  of  the  left  ventricle 
(weight  70  gm.)  ;  hypertrophy  and  dilatation  of  the  right  auricle,  and  concentric 
hypertrophy  and  chronic  mural  endocarditis  of  the  left  auricle;  chronic  mitral 
endocarditis  (extreme  stenosis  and  thickening,  with  sclerosis  of  chordae  ten- 
dineae  and  tips  of  papillary  muscles)  ;  acute  fibrinous  pericarditis,  and  (slight) 
acute  vegetation  mitral  and  mural  endocarditis.;  chronic  fibrous  pleurisy  and 
pericarditis  (basal)  ;  general  chronic  passive  congestion  of  viscera;  hydrothorax 
(bilateral)  and  ascites.  Histologic  examination  confirmed  these  findings  and 
showed  surprisingly  little  myocardial  fibrosis. 

Summary  of  Case. — A  boy  of  18,  suffering  with  mitral  stenosis, 
was  admitted  to  the  hospital  in  an  extreme  stage  of  decompensation,  but 
with  normal  cardiac  rhythm.  His  condition  became  steadily  worse  and 
eventually  auricular  fibrillation  developed,  and  the  next  day  an  acute 
pericarditis  was  found  to  be  present.  Fibrillation  was  replaced  after 
three  days  by  normal  rhythm,  but  death  occurred  four  days  later  from 
cardiac  failure  with  persistence  of  the  acute  pericarditis.  At  autopsy 
an  extreme  mitral  stenosis,  with  cardiac  hypertrophy  and  dilatation  was 
found. 

V.   DEVELOPMENT   OF    PERMANENT   AURICULAR    FIBRILLATION 

In  two  cases  the  onset  of  auricular  fibrillation  occurred  while  the 
patient  was  under  observation.  Although  the  first  attack  in  each  of 
these  cases  proved  to  be  permanent,  they  are  included  in  this  series  on 
account  of  certain  prognostic  indications  that  they  offer. 

CASE  5. — L.  Z.,  a  Polish  woman,  33  years  old,  married,  was  admitted  to  the 
maternity  ward  of  the  University  Hospital,  Jan.  6,  1915,  in  her  fourth  preg- 
nancy. The  first  three  pregnancies  were  normal,  but  after  the  birth  of  the 
third  child,  she  had  a  severe  attack  of  "grippe."  was  in  bed  after  that  for 
three  months,  and  was  told  by  her  doctor  at  that  time  that  she  had  heart 
trouble.  She  had  had  scarlet  fever,  measles,  chickenpox  and  typhoid  as  a 
child,  but  had  never  had  sore  throat,  acute  rheumatic  fever,  or  any  symptoms 
of  heart  disease.  Her  social  and  family  histories  were  negative. 

Her  present  attack  of  decompensation  began  about  the  seventh  month  and 
gradually  grew  worse  as  pregnancy  progressed,  until  in  the  ninth  month  labor 
was  induced  by  Dr.  Hirst  on  account  of  extreme  dyspnea  and  edema.  After 
delivery  her  symptoms  were  much  improved,  but  one  week  later  an  attack  of 
intense  dyspnea  ensued,  with  precordial  pain  and  a  dry,  nonproductive  cough. 
She  also  suffered  from  anorexia,  constipation,  headache,  weakness,  and  pain  in 
both  breasts  (baby  had  been  weaned  two  days  before). 

Physical  Examination. — When  transferred  to  the  medical  ward,  the  usual 
signs  of  marked  decompensation  were  found.  The  pulse  was  regular,  rapid, 
quick,  fair  volume  and  tension  and  the  wall  of  the  artery  not  sclerosed.  The 
systolic  blood  pressure  was  130,  the  diastolic  80.  There  were  forcible  arterial 
pulsations  in  the  neck,  with  apparently  the  ventricular  type  of  venous  pulse. 
The  cardiac  impulse  was  forcible,  17  cm.  from  the  midline  (following  curve  of 
chest),  almost  in  midaxilla,  in  the  fifth  interspace.  The  cardiac  dulness  extended 
5  cm.  to  the  right  of  the  midline,  17  cm.  to  the  left.  At  the  apex  the  first 
sound  was  loud  and  preceded  by  a  presystolic  murmur  and  thrill,  a  systolic 


20 

murmur  also  being  heard  nearer  the  sternum.  The  second  pulmonic  was 
accentuated,  the  liver  enlarged  and  palpable  and  rales  audible  at  the  bases  of 
the  lungs.  There  was  generalized  edema,  ascites  and  bilateral  hydrothorax. 
The  blood  showed  a  moderate  anemia.  The  specific  gravity  of  the  urine  was 
1.028,  and  it  contained  a  cloud  of  albumin,  and  hyaline,  granular  and  leukocytic 
casts.  The  phenolsulphonephthalein  elimination  was  47  per  cent.  The  Was- 


Fig.  14  (Case  5). — Electrocardiogram  of  patient  L.  Z.,  a  case  of  fatal  mitral 
stenosis  with  decompensation,  taken  Jan.  8,  1916,  showing  normal  rhythm  with 
right  ventricular  preponderance. 

sermann  reaction  was  negative.  An  electrocardiogram  (Fig.  14)  showed  a 
regular  rhythm  with  preponderance  of  the  right  ventricle  and  poorly  defined 
T  waves. 

Course. — The  patient  improved  slightly  under  digitalis  and  hypnotics,  but 
four  days  after  admission  she  had  another  attack  of  dyspnea  and  tachycardia. 
The  pulse  at  the  wrist  was  uncountable,  the  heart  rate  by  auscultation  was  196 
and  apparently  regular.  The  following  day,  after  a  good  night's  rest,  the 


21 

patient  seemed  much  better  and  the  pulse  rate  was  lower.  The  day  after  this, 
arrhythmia  was  first  noted,  and  the  electrocardiograph  (Fig.  15)  established 
the  diagnosis  of  auricular  fibrillation.  Although  there  is  no  record  of  the 
heart  rhythm  on  the  intervening  day,  it  is  probable  that  the  rapid  period 
was  due  to  auricular  flutter,  which  progressed  to  fibrillation.  The  course  of 
the  physical  signs  and  several  electrocardiograms  taken  in  the  next  few  days 


J>To. 


3. 


Fig.  15  (Case  5). — Electrocardiogram  of  same  patient  as  in  Figure  14,  taken 
January  14,  showing  permanent  auricular  fibrillation.  Though  this  symptom 
has  not  been  of  long  duration,  the  waves  of  fibrillation  are  not  visible. 

confirmed  the  diagnosis  of  fibrillation  and  recorded  the  response  of  the  heart 
to  digitalis  (slowing  of  rate,  lessening  of  arrhythmia,  change  in  form  and  Q 
and  T  waves).  At  no  time  were  the  waves  of  fibrillation  of  the  coarse  type. 
The  patient,  however,  failed  to  improve  clinically,  and  succumbed  in  three  days 
with  the  signs  of  acute  dilatation.  Necropsy  was  refused. 

Summary  of  Case. — A  woman  with  mitral  stenosis  of  at  least  four 
years'  duration  had  such  severe  signs  of  decompensation  during  her 
fourth  pregnancy  that  labor  had  to  be  induced.  She  improved  during 
the  first  week  of  the  puerperium,  but  then  a  second  and  more  severe 


22 

stage  of  decompensation  set  in.  In  the  third  day  of  this  attack  a  very 
rapid  pulse  rate  was  initiated  (auricular  flutter?)  and  this  progressed 
to  auricular  fibrillation,  which  persisted  until  death  three  days  later. 
The  development  of  auricular  fibrillation  after  a  transient  period  of 
flutter  has  been  frequently  observed ;  in  fact  the  administration  of  large 
doses  of  digitalis  has  been  recommended  in  cases  of  auricular  flutter 
in  the  hope  that  the  disturbance  may  pass  on  to  fibrillation  and  thence, 
perhaps,  return  to  normal  rhythm.  The  contingency  must  at  least  be 
considered,  therefore,  in  the  present  case  that  digitalis  was  a  con  • 
tributing  factor  to  the  causation  of  fibrillation. 

VI.  DEVELOPMENT  OF  PERMANENT  AURICULAR  FIBRILLATION  DURING 
CARDIAC  DECOMPENSATION 

Another  case  is  reported  in  which  auricular  fibrillation  developed 
after  three  years  occasional  observation. 

CASE  6. — M.  H.,  an  American  woman,  35  years  old,  married,  was  admitted 
to  the  University  Hospital  on  March  21,  1916,  with  the  usual  signs  and  symp- 
toms of  cardiac  decompensation.  This  was  a  recurrence  similar  to  those  seen 
in  her  previous  admissions  in  the  spring  of  1913  and  the  autumn  of  1914.  She 
had  had  measles,  mumps,  scarlet  fever  and  acute  articular  rheumatism.  Her 
cardiac  symptoms  were  first  noted  at  the  time  of  a  second  attack  of  acute 
polyarthritis  thirteen  years  before,  and  reappeared  during  an  attack  of  "grippe" 
nine  years  before.  For  the  past  four  years  she  has  suffered  from  some 
shortness  of  breath  and  puffiness  of  the  ankles,  which  on  the  two  occasions 
mentioned  became  bad  enough  to  make  her  seek  the  hospital.  At  both  these 
times  she  improved  quickly  under  hospital  care,  and  she  had  never  noticed  any 
irregularities  of  her  heart  further  than  an  occasional  dropped  beat. 

The  present  illness  started  two  weeks  before  admission  with  greatly  increased 
dyspnea,  palpitation  and  pericardial  pain.  Four  days  later  the  patient  suffered 
a  "stroke,"  losing  the  power  of  speech  and  of  moving  the  left  arm,  but  not 
becoming  unconscious.  Speech  returned  after  sleep,  but  the  left  thumb,  index 
finger  and  left  side  of  the  face  have  remained  numb  and  weak.  Four  days 
after  that,  sudden  pain  developed  low  in  the  right  chest  with  cough  and  hemop- 
tysis, and  the  lesion  was  later  shown  by  the  Roentgen  ray  to  be  a  pulmonary 
infarct.  Social  and  family  history  irrelevant. 

Physical  Examination. — It  was  found  on  examination  that  the  patient  was 
more  emaciated  than  on  previous  admissions ;  the  tongue  was  dry  and  coated, 
with  herpes  on  the  lips.  The  cardiac  dulness  extended  3  cm.  to  the  right  of 
the  midline  and  13  cm.  to  the  left.  The  apex  beat  was  well  localized  in  the 
fifth  space  2  cm.  outside  of  the  midclavicular  line.  There  was  a  harsh  systolic 
murmur,  best  heard  at  the  apex  and  transmitted  to  the  base  and  axilla.  No 
arrhythmia  was  noted.  The  liver  was  palpable  4  cm.  below  the  costal  margin 
and  the  right  kidney  was  also  palpable.  There  was  dulness  and  rales  at  the 
bases  of  both  lungs,  but  more  marked  on  the  right.  The  leukocytes  varied 
between  10,000  and  14,000;  hemoglobin  95  per  cent.,  red  blood  cells  5,480,000. 
The  urine  was  acid,  specific  gravity  1.018,  contained  a  cloud  of  albumin,  urates, 
but  no  casts.  The  Wassermann  reaction  was  negative.  The  systolic  blood 
pressure  varied  between  115  and  120,  the  diastolic  between  77  and  90.  The 
signs  of  decompensation  decreased  steadily  during  the  patient's  stay  in  the 
hospital,  so  that  she  was  able  to  leave  in  one  month  in  very  good  condition. 
The  cardiac  arrhythmia,  which  was  first  discovered  by  electrocardiographic 
examination,  was  still  present,  but  frequently  had  been  so  slight  that  it  could 
not  be  detected  by  simple  digital  examination  of  the  pulse. 


Fig.  16  (Case  6). — Electrocardiogram  of  patient  M.  H.,  a  case  of  mitral 
stenosis  with  decompensation,  taken  April  14,  1913,  showing  normal  rhythm 
(sinus  arrhythmia). 


Fig.  17  (Case  6). — Electrocardiogram  of  same  patient  as  in  Figure  16,  taken 
in  November,  1914.  The  figure  shows  occasional  auricular  premature  con- 
tractions. 


24 

Electrocardiograms  (Fig.  16)  were  taken  during  each  stay  at  the  hospital. 
The  one  taken  in  1913  showed  a  normal  rhythm  and  complexes,  with  a  P-R 
interval  of  0.18  second.  No  abnormalities  of  rhythm  were  noted  either  dur- 
ing the  examination  or  during  the  patient's  stay  in  the  hospital.  The  electro- 
cardiogram (Fig.  17)  taken  in  1914  showed,  besides  some  small  changes  in  the 
form  of  the  ventricular  complex,  the  same  P-R  interval  as  on  the  first  admis- 
sion, but  two  definite  auricular  extrasystoles  in  addition.  The  large  P  wave 


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Fig.  18  (Case  6). — Electrocardiogram  of  same  patient  as  in  Figure  16.  show- 
ing permanent  auricular  fibrillation   (waves  of  coarse  type). 

characteristic  of  mitral  stenosis  persisted.  On  the  patient's  last  admission  in 
March,  1916,  electrocardiograms  (Fig.  18)  taken  on  several  occasions  con- 
stantly showed  a  coarse  type  of  auricular  fibrillation.  The  form  of  the  ven- 
tricular complexes,  however,  had  changed  very  little  from  that  of  the  two 
former  admissions.  Although  the  patient  improved  steadily  from  a  clinical 
point  of  view,  fibrillation  persisted  with  a  gradual  decrease  of  the  coarseness 
of  the  fibrillation  waves. 


25 

Summary  of  Case. — In  a  case  of  mitral  stenosis  of  some  years' 
standing  with  recurrent  periods  of  decompensation*  electrocardio- 
graphic  records  were  made  over  a  period  of  three  years.  At  first  the 
rhythm  was  normal,  next  was  broken  by  occasional  auricular  extra- 
systoles  and  finally  was  found  to  have  been  replaced  by  a  constant, 
coarse  type  of  fibrillation.  If  the  history  may  be  relied  upon,  this  prob- 
ably developed  within  two  weeks  of  admission  to  the  hospital,  when 
decompensation  was  further  complicated  by  cerebral  and  pulmonary 
emboli  and  infarct  formation. 

GENERAL  COMMENT 

A  comparison  of  the  foregoing  cases  with  those  mentioned  in  the 
literature  allows  the  change  from  normal  rhythm  to  auricular  fibrilla- 
tion to  be  subdivided  into  three  types. 

In  the  first  group  falls  the  first  case  of  this  series,  twelve  of  Cohn's11 
pneumonia  cases,  all  four  of  those  reported  by  Fahrenkamp,  Robin- 
son's12 recent  case,  the  fourth  of  Heitz's  and  the  sixth  of  Fox's  series. 
In  these  cases  the  predominant  factor  was  some  acute  infection  or 
intoxication  (pneumonia,  Septicemia,  hyperthyroidism),  and  the  attack 
of  fibrillation  was  single.  No  organic  cardiac  lesion  was  found  or  need 
be  presumed,  and  when  the  infection  or  intoxication  was  removed  the 
rhythm  returned  permanently  to  normal. 

In  the  second  group,  and  this  comprises  the  larger  number  of  those 
cases  reported  as  paroxysmal  auricular  fibrillation,  belong  the  second 
and  probably  the  third  cases  of  this  report,  also  the  remaining  nine  of 
Heitz's,  the  four  of  Hornung's,  four  of  Fox's  series,  and  the  single  cases 
of  Robinson,  Popper,  and  Lewis  and  Schleiter.  At  the  time  of  observa- 
tion all  but  three  of  these  patients  were  in  the  sixth  or  seventh  decade  of 
life,  but  the  onset  of  attacks  when  mentioned  occurred  as  follows :  Two 
in  the  third  decade,  two  in  the  fourth,  five  in  the  fifth,  five  in  the  sixth, 
and  six  in  the  seventh  decade.  The  average  duration  of  the  condition 
was  over  nine  years.  Both  sexes  were  equally  involved.  Previous  dis- 
eases bore  no  relationship  to  the  condition ;  even  the  cardiac  condition 
varied  greatly.  In  eight  cases  mitral  lesions  were  present,  but  in  ten 
others  no  valvular  lesion  was  found.  In  nearly  all,  however,  there  was 
distinct  evidence  of  myocardial  disease.  The  blood  pressure  was  found 
increased  in  seven  and  not  increased  in  eight.  Arteriosclerosis  was 
noted  in  ten.  Factors  determining  the  paroxysms  were  either  absent  or 
widely  varying  in  character.  In  six,  emotional  excitement  preceded 
attacks  and  in  two  others  they  were  attributed  to  a  general  increase  in 


11.  Cohn,  A.  E. :    Certain  Phases  of  the  Action  of  Digitalis  in  Pneumonia, 
Meeting  of  Am.  Soc.  for  the  Advancement  of  Clin.  Investigations,  Washington, 
D.  C,  May  8,  1916,  unpublished. 

12.  Robinson,  G.  C. :   Transient  Auricular  Fibrillation  in  a  Healthy  Man  Fol- 
lowing Hydrogen  Sulphid  Poisoning,  Jour.  Am.  Med.  Assn.,  1916,  Ixvi,  1611. 


26 

the  patient's  nervousness.  In  four,  attacks  were  induced  by  exercise  or 
fatigue,  but  in  three  others  they  nearly  always  occurred  during  sleep. 
Overeating  (three  cases),  defecation,  and  asthmatic  attacks  were  held 
responsible  in  other  cases.  Many  of  these  factors  might  be  grouped 
under  the  head  of  conditions  that  raise  blood  pressure,  but  in  some 
cases  this  factor  was  definitely  absent.  The  duration  of  the  individual 
attacks  was  also  extremely  variable,  ranging  from  a  few  minutes  to 
several  weeks;  in  most  cases,  however,  they  lasted  a  few  hours.  In 
the  early  stages  the  attacks  tended  to  be  either  short  or  infrequent,  the 
duration  and  frequency  of  the  attacks  increasing  as  the  disease 
progressed.  They  usually  began  abruptly,  without  premonitory  symp- 
toms, and  caused  more  or  less  severe  cardiac  embarrassment.  The 
attacks  ended  either  during  sleep  or  with  such  abruptness  that  the 
patient  could  notice  the  return  to  regular  rhythm.  In  only  one  case 
were  extrasystoles  noticed  between  attacks,  and  in  two  cases  there 
occurred  also  attacks  of  paroxysmal  tachycardia.  In  this  connection 
Lewis  and  Schleiter  have  called  attention  to  the  closely  related 
mechanism  of  auricular  extrasystoles,  fibrillation  and  paroxysmal 
tachychardia.  Six  patients  died  while  under  observation  (mostly 
from  cardiac  complications  during  regular  rhythm)  ;  in  five  others 
fibrillation  had  become  permanent;  while  six  of  the  remaining 
ten  were  considered  as  improved.  Venesection,  digitalis  and  quinin 
have  been  used  successfully  and  the  ordinary  treatment  of  cardiac 
failure  seems  advisable. 

In  a  third  group,  represented  by  the  last  three  cases  of  this  report 
and  the  fourth  of  Fox's  series,  the  onset  of  fibrillation  should  be 
regarded  as  but  one  more  link  in  the  chain  of  cardiac  failure.  In  all 
these  cases  the  signs  of  mitral  disease  with  decompensation  were  prom- 
inent and  had  existed  for  years.  In  two  cases  the  first  attack  of  fibrilla- 
tion proved  to  be  permanent,  one  of  these  being  preceded  by  auricular 
extrasystoles,  in  one  other  the  permanent  period  was  preceded  by  one 
transient  period,  and  in  the  fourth  a  transient  period  lasting  three  days 
occurred  a  few  days  before  death  from  cardiac  failure  (normal 
rhythm).  The  development  of  most  of  the  cases  of  permanent  auricu- 
lar fibrillation  is  probably  of  this  character,  but  closer  observation  and 
wider  use  of  graphic  methods  would  probably  reveal  one  or  more  pre- 
vious transient  periods.  As  auricular  fibrillation  aggravates  the  prog- 
nosis, energetic  treatment  should  be  instituted  at  these  times,  in  order 
to  delay  or  avoid  the  onset  of  the  permanent  condition.  That  this 
should  not  include  too  large  doses  of  digitalis  is  indicated  by  the  fact 
that  in  two  cases  at  least  (Case  3  of  this  report  and  Robinson's  case) 
digitalis  was  considered  as  a  possible  factor  in  the  production  of  fibril- 
lation. Its  value  as  a  cardiac  remedy,  however,  especially  after  fibril- 
lation is  established,  makes  it  a  necessary  aid  in  practically  all  such 
cases. 


27 

SUMMARY 

Four  cases  are  described  in  which  the  transition  of  the  cardiac 
mechanism  was  observed  from  normal  rhythm  to  auricular  fibrillation 
and  back  again.  In  two  others  the  development  of  permanent  auricular 
fibrillation  was  observed.  These  have  been  compared  with  similar 
cases  in  the  literature. 

CONCLUSIONS 

Transient  auricular  fibrillation  is  a  comparatively  rare  condition, 
although  the  more  widespread  and  frequently  repeated  use  of  the  string , 
galvanometer  will  probably  reveal  many  more  cases  than  are  now 
available  for  study. 

The  change  from  normal  rhythm  to  auricular  fibrillation  occurs 
in  three  well-defined  groups: 

1.  In  the  course  of  an  acute  infection,  such  as  pneumonia  or  septi- 
cemia,  or  of  an  acute  intoxication,  such  as  alcohol  or  hyperthyroidism, 
or  possibly  from  other  temporary  causes,  one  or  more  attacks  of  fibril- 
lation may  occur  for  several  days,  but  disappear  permanently  when  the 
source  of  intoxication  is  removed.    In  this  group  permanent  myocardial 
damage  is  probably  not  present. 

2.  In  another  group,  probably  always  associated  with  underlying 
myocardial  degeneration,  paroxysms  lasting  from  a  few  minutes  to 
many  hours  or  even  days,  may  be  induced  by  a  great  variety  of  causes 
and  occur  over  a  period  of  many  years.    They  tend,  however,  to  become 
more  lasting  or  more  frequent  or  both,  and  eventually  with  the  progress 
of  the  myocardial  disease  the  fibrillation  becomes  permanent.     Death 
may  occur,  however,  before  permanent  fibrillation  has  ensued,  or  clin- 
ical improvement  may  take  place  with  the  onset  of  fibrillation.     The 
term  "paroxysmal"  is  most  aptly  applied  to  cases  of  this  group. 

3.  In  a  third  group,  in  which  the  signs  of  valvular  or  myocardial 
disease  are  more,  prominent,  the  original  change  from  normal  rhythm 
to  fibrillation  is  liable  to  be  permanent,  or  at  least  be  preceded  by  only 
a  few  transient  periods.    A  determining  factor  in  such  cases  is  liable 
to  be  some  cardiac  complication,  such  as  pulmonary  embolus,  acute 
pericarditis,  or  the  added  strain  of  pregnancy,  and  may  be  preceded  by 
a  transient  period  of  flutter. 

No  relationship  between  the  onset  of  fibrillation  and  changes  in 
blood  pressure  could  be  established. 

In  the  earlier  stages  of  fibrillation  the  electrocardiogram  usually 
shows  coarser  waves  of  fibrillation,  so  that  this  evidence,  when  pres- 
ent, may  be  guardedly  used  to  influence  favorably  the  prognosis. 


28 

The  occurrence  of  fibrillation,  while  a  bad  factor  in  prognosis,  does 
not  necessarily  indicate  either  permanency  or  a  fatal  outcome.  It  is 
of  graver  significance  when  it  occurs  in  valvular  cases  with  prominent 
signs  of  decompensation,  and  of  least  significance  in  the  cases  of  the 
first  group. 

The  usual  treatment  of  heart  failure  (rest  in  bed,  the  digitalis 
group,  removal  of  sources  of  intoxication,  etc.)  help  to  terminate 
attacks  of  fibrillation,  but  excessive  doses  of  digitalis  may  help  to 
induce  this  condition. 

These  cases  were  studied  in  the  wards  and  laboratory  of  the  University 
Hospital,  while  under  the  care  of  Drs.  Stengel,  Hirst,  Anspach  and  Newlin,  to 
whom  my  thanks  are  due. 


UNIVEESITY   OF    CALIFOENIA   LIBEAEY, 
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